2016
DOI: 10.1007/978-3-319-41523-9_14
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Adhesion GPCR Function in Pulmonary Development and Disease

Abstract: Classic G-protein-coupled receptors (GPCRs) control multiple aspects of pulmonary physiology as demonstrated by loss-of-function experiments in mice and pharmacologic targeting of GPCRs for treatment of several pulmonary diseases. Emerging data demonstrate critical roles for members of the adhesion GPCR (aGPCR) family in pulmonary development, homeostasis, and disease. Although this field is still in its infancy, this chapter will review all available data regarding aGPCRs in pulmonary biology, with a particul… Show more

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Cited by 13 publications
(9 citation statements)
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“…Full-length ADGRF1 was reported to be activated by synaptamide, a metabolite of the omega-3 fatty acid docosahexaenoic acid in brain tissue (77). Mice lacking ADGRF5 and surfactant protein D phenocopy each other in lung tissue and it has been found that surfactant protein D can interact the with ectodomain of F5 (78). However, as for many of the interactions described in this section, it is not yet clear what effect this interaction may have on G protein signaling or other signaling downstream of F5 (79).…”
Section: Adhesion Gpcr Ligandsmentioning
confidence: 99%
“…Full-length ADGRF1 was reported to be activated by synaptamide, a metabolite of the omega-3 fatty acid docosahexaenoic acid in brain tissue (77). Mice lacking ADGRF5 and surfactant protein D phenocopy each other in lung tissue and it has been found that surfactant protein D can interact the with ectodomain of F5 (78). However, as for many of the interactions described in this section, it is not yet clear what effect this interaction may have on G protein signaling or other signaling downstream of F5 (79).…”
Section: Adhesion Gpcr Ligandsmentioning
confidence: 99%
“…Since both Gnaq and Gna11 are expressed in mouse AT2 cells (45) and demonstrate functional redundancy in several tissues (46, 47), we employed a strategy to delete Gnaq and Gna11 in mouse AT2 cells using the SftpcCreER driver. SftpcCreER-specific deletion of Gnaq on a Gna11-deficient background resulted in a 9-fold increase in alveolar surfactant pools ( Figure 6E), consistent with the pulmonary phenotype in ShhCre:Gpr116…”
Section: Gpr116mentioning
confidence: 99%
“…The reader can see that among the extracted features the ADGRF5 gene with Ensembl ID ENSG00000069122.17 is the one that occurs most in the classification rules. Previous studies have already shown that mutations within this gene are possible causes of lung cancer (LUSC) [ 42 ]. Similarly, many other genes extracted from the classification rules of LUSC are listed in several publications that concern this tumor [ 43 ].…”
Section: Resultsmentioning
confidence: 99%